Hemorrhoids are normal vascular and connective-tissue cushions of the anal canal. The term hemorrhoidal disease (HD) refers to these cushions when they become symptomatic.^[1] According to the current “sliding anal cushion” model, the supporting connective tissue and smooth muscle weaken with age and straining. The cushions then prolapse, become engorged, and bleed. This model has replaced the older view of hemorrhoids as varicose veins.^[2][3] Hemorrhoids are classified relative to the dentate line as internal, external, or mixed. Internal hemorrhoids are further graded I–IV by degree of prolapse using the Goligher classification.^[4] Internal hemorrhoids have visceral innervation, so they typically cause painless bleeding and prolapse. External hemorrhoids have somatic innervation and become painful when thrombosed.^[1]

HD is the most common anorectal disorder in adults, with an estimated global pooled prevalence of about 26%. In the United States, it affects approximately 10 million people and accounts for nearly 4 million office and emergency department visits each year.^[5][6] The most consistent risk factors are constipation with straining or prolonged toilet sitting, increasing age, and pregnancy. Common symptoms include hematochezia, prolapse, anal discharge, and pain when an external hemorrhoid thromboses. Diagnosis is made by inspection, digital rectal examination, and anoscopy. Rectal bleeding or anemia should not be attributed to hemorrhoids until colorectal cancer and other sources have been excluded.^[7]

Treatment escalates by grade. First-line therapy for all grades is increased dietary fiber and fluid intake with correction of defecation habits. Rubber band ligation is the first-line office procedure for grade I–III internal hemorrhoids. Excisional hemorrhoidectomy is the most durable option for refractory grade III, grade IV, and mixed disease.^[4] HD usually follows a relapsing–remitting course with an excellent prognosis, and only about 10% of patients ultimately require surgery.^[1]

Hemorrhoids were first documented by ancient Egyptians more than 3,700 years ago.

Hemorrhoids are classified by anatomic origin relative to the dentate line as internal, external, or mixed. Internal hemorrhoids are further graded I–IV by degree of prolapse using the Goligher classification. Grade I bleeds without prolapse; grade IV is irreducible. Location and grade together determine the stepwise escalation from conservative therapy to office-based procedures to surgery. External hemorrhoidal disease is not graded and becomes clinically relevant mainly when acutely thrombosed.^[1][4]

Hemorrhoids are normal vascular and connective-tissue cushions of the anal canal; the term hemorrhoidal disease refers to these cushions when they become symptomatic.^[1][8] The dominant current model is the “sliding anal cushion” theory, which replaced the older idea that hemorrhoids are varicose veins. In this model, the connective tissue and smooth muscle that anchor the cushions weaken. The cushions then slide downward (prolapse), become engorged, and bleed.^[2][3] Bleeding from hemorrhoids is arterial in character because it comes from arteriovenous communications within the cushions. This is the rationale for artery-directed therapies.^[2] The dentate line marks the boundary between the two types and explains their different symptoms. Internal hemorrhoids have visceral innervation, so they bleed and prolapse painlessly. External hemorrhoids have somatic innervation, so they are painful when thrombosed.^[1]

No single cause has been identified. Disease reflects risk factors acting through two linked mechanisms: degeneration of the supporting tissue, and increased anorectal or intra-abdominal venous pressure.^[9][1] The best-supported associations are:

• Disordered defecation, including constipation, straining, and prolonged toilet sitting
• Increasing age
• Pregnancy and parity
• Smoking and hypertension, which are small but independent correlates in large screening data^[10]

The roles of obesity, diet, physical activity, diarrhea, and portal hypertension remain inconsistent. Anatomic hemorrhoids are common and often asymptomatic. Associations derived from endoscopic prevalence studies therefore may not apply directly to symptomatic disease.^[11]

Hemorrhoids should be differentiated from other diseases that cause anal discomfort and pain with defecation such as rectal cancer, anal fissure, anal abscess, and anal fistula.

Hemorrhoidal disease (HD) is the most common anorectal disorder in adults and one of the most frequent outpatient gastrointestinal diagnoses.^[12][6] Reported prevalence ranges from about 4% to nearly 40%. Most of this spread comes from differences in case definition and ascertainment method (self-report, physician examination, or endoscopy), not from true biological differences between populations.^[5][13]

• The largest meta-analysis to date covered 150 studies and about 9 million individuals. It estimated a global pooled point prevalence of approximately 26%.^[5]
• Prevalence rises with age and is modestly higher in women, mainly because of pregnancy and parity.^[5][10]
• In the United States, HD affects approximately 10 million people. It accounts for nearly 4 million office and emergency department visits each year.^[1][6]
• True prevalence is unknown, because many affected individuals are asymptomatic or self-treat and never seek care.^[5][6]

Current models attribute it mainly to age- and strain-related degeneration of the supporting connective tissue and anchoring (Treitz) muscle, with vascular engorgement as a secondary feature. This replaces the older varicose-vein (venous stasis) model.^[3][14] The most consistent risk factors are increasing age, constipation with straining or hard stools, and the late-pregnancy and peripartum period. Prior HD is a strong predictor of HD during pregnancy. Higher adiposity has genetic support for a causal role, even though observational data are inconsistent.^[10][15]. In cirrhosis with portal hypertension, HD is more prevalent but must be distinguished from rectal varices, which are a separate entity.^[16]

According to the USPSTF, screening for hemorrhoids is not recommended.

Most symptomatic hemorrhoids follow a relapsing–remitting course with an excellent overall prognosis, and only about 10% of patients ultimately require surgery.^[1] Asymptomatic or incidentally detected hemorrhoids need no treatment.^[1][3] The main complications of the disease are thrombosis of external hemorrhoids, strangulation of irreducible (grade IV) prolapse with risk of gangrene and perineal sepsis, iron-deficiency anemia from chronic bleeding, and pruritus ani with soiling.^[14][7] Treatment-related complications include pain and delayed bleeding after rubber band ligation, and urinary retention, fecal incontinence, and anal stricture after hemorrhoidectomy. Perineal sepsis after office procedures is rare but can be fatal.^[4] Recurrence rises as treatment becomes less invasive. Excisional hemorrhoidectomy has the lowest recurrence (2%–10%), and its advantage over rubber band ligation is concentrated in grade III disease.^[1][17][18] Rectal bleeding or anemia should never be attributed to hemorrhoids until colorectal cancer and other sources have been excluded.^[7]

Symptoms of hemorrhoids include pain with defecation, hematochezia, and anal discharge.

Patients with acute prolapsed or thrombosed hemorrhoids usually appear ill and in pain. Physical examination of patients with hemorrhoids is usually remarkable for protruding mass from the anus or palpable mass on digital rectal exam.

There are no specific diagnostic lab findings associated with hemorrhoids. However, complete blood count may show anemia in the case of chronic bleeding.

There are no X-ray, MRI or ultrasound findings associated with hemorrhoids.

There are no other diagnostic imaging studies of significance for hemorrhoids.

Anoscopy is mandatory to visualize internal hemorrhoids as they are not visible on inspection of the anal verge or palapable on performing digital rectal exam.

Medical (non-procedural) therapy is the appropriate initial management for symptomatic hemorrhoidal disease of all grades and is often definitive for grade I–II internal hemorrhoids.^[14][12] Increased dietary fiber and fluid intake with correction of defecation habits is first-line therapy with the strongest supporting evidence; it reduces persistent symptoms and bleeding but does not improve prolapse, pain, or pruritus.^[4][19] Topical preparations are low-risk symptomatic adjuncts supported only by low-quality evidence.^[4] Oral flavonoid phlebotonics reduce bleeding, pruritus, and discharge in randomized trials, but symptoms frequently recur after discontinuation and these agents are not FDA-approved in the United States.^[20][1] Patients who fail an adequate trial of medical therapy, or who have high-grade prolapse, should be referred for office-based procedures or surgery.^[3]

Procedural treatment of hemorrhoidal disease is reserved for symptomatic internal hemorrhoids that fail conservative therapy and for selected external or mixed disease. Conservative therapy includes dietary fiber 20–30 g/day, adequate fluid intake, avoiding straining and prolonged toilet sitting, and optional phlebotonics. Treatment escalates by grade, starting with the least invasive option. Office-based procedures are used for grade I–III internal hemorrhoids. Surgery is used for refractory grade III, grade IV, mixed internal–external disease, and acutely thrombosed external hemorrhoids.^[1][3][4] About 10% of patients with hemorrhoidal disease eventually undergo surgery.^[1] Rubber band ligation is the first-line office procedure. Excisional hemorrhoidectomy is the most durable operation but causes the most postoperative pain. Non-excisional techniques, such as Doppler-guided hemorrhoidal artery ligation, laser hemorrhoidoplasty, and radiofrequency ablation, cause less pain but have higher recurrence rates. Stapled hemorrhoidopexy is not recommended as routine first-line surgery.^[4][21]

Primary prevention of hemorrhoids may include drinking excessive fluids, regular exercise, practicing better posture, and reduction of bowel movement straining and time. Eating a high-fiber diet can make stools softer and easier to pass, reducing the pressure on hemorrhoids caused by straining.

The secondary preventive measures for hemorrhoids are similar to primary preventive measures.